CARDIOPULMONARY

PHYSICAL THERAPY
LEC-01
Reference book : Cardiopulmonary physical therapy 3rd edition
Donna frownfelter
Chapter :02
Topic :
ANATOMY AND PHYSIOLOGY OF CARDIAC SYSTEM
 Outline
Heart and diaphragm
Pericardium and its division
Layers of heart
Arterial & nerve supply of heart
Surface marking of Heart
Cardiac physiology :Starling , Anrep and Bowdich
effects
Heart sounds
Respiratory acidosis and alkalosis
 ANATOMY OF HEART
 The heart is a conical, hollow muscular pump enclosed in a
fibroserous sac, the pericardium.

 Its size is closely related to body size and corresponds

remarkably to the size of an individual's clenched fist.

 It is positioned in the center of the chest behind the lower half of

the sternum.

 The largest portion of the heart lies to the left of the midsternal
line; the apex is found approximately 9 cm to the left in the fifth
intercostal space.
ANATOMY OF HEART
 The heart as a whole is freely movable within the
pericardial cavity, changing position during both
contraction and respiration.

 During contraction, the apex moves forward, strikes the

chest and imparts the chest and apex beat, which may be
felt and seen.

 Abnormal position of the apex beat can indicate cardiac

enlargement or displacement.
 ANATOMY OF HEART
During breathing, the movements of the diaphragm determine
the position of the heart. This is because of the attachment of
the central tendon of the diaphragm to the pericardium.

Changes in position during quiet breathing are hardly

noticeable, but with deep inspirations, the downward
excursion of the diaphragm causes the heart to descend and
rotate to the right. The opposite occurs during expiration.

Pathology of the lungs can also change the position of the

heart.
ANATOMY OF HEART
Atelectasis shifts the heart to the same side.

In tension pneumothorax, where air enters the chest

usually through an opening in the chest wall and
cannot escape, the positive pressure shifts the heart
away from the side of the pathology.
ANATOMY OF HEART
The outer surface, a tough fibrous membrane, is
called the fibrous pericardium.

It encases the heart and the organs and terminations of

the great vessels. This membrane is so unyielding that
when fluid accumulates rapidly in the pericardial
cavity, it can compress the heart and impede venous
return.

The inner surface, the serous pericardium, is a

serous membrane that lines the fibrous pericardium.
ANATOMY OF HEART
Ten to 20 ml of clear pericardial fluid separates and
moistens the two pericardial surfaces.

The pericardium with its fluid minimizes friction

during contraction. It also holds the heart in position
and prevents dilation.

The serous pericardium consists of an outer layer, the

parietal layer, and an inner layer the visceral layer, or
epicardium
ANATOMY OF HEART
 The heart is divided into three layers-the epicardium,
myocardium, and endocardium.

 The outermost layer, the epicardium, is visceral

pericardium and is often infiltrated with fat. The coronary
blood vessels that nourish thee heart run in this layer before
entering the myocardium.

 The myocardium consists of cardiac muscle fibers. The

thickness of the layers of cardiac muscle fibers is directly
proportional to the amount of work they perform.
ANATOMY OF HEART
 The ventricles do more work than the atria, and their walls
are thicker. The pressure in the aorta is higher than that in
the pulmonary trunk. This requires greater work from the
left ventricle, so its walls are twice as thick as those of the
right ventricle.

 The innermost layer, the endocardium, is the smooth

endothelial lining of the interior of the heart.
ANATOMY OF HEART
 The Valves of the heart, although delicate in appearance,
are designed to withstand repetitive closures against high
pressures (French, Criley, 1983).

 Normally, they operate for more than 80 years without need

of repair or replacement.

 The tricuspid and mitral valves function differently from

the other valves of the heart.
ANATOMY OF HEART
 During diastole, the two leaflets or cusps of the mitral valve
and the three cusps of the tricuspid valve relax into the
cavities of the ventricles, allowing blood to flow between
the two chambers.

 As the ventricular chambers fill with blood, the cusps of the

valves are forced up into a closed position.

 Fibrous cords, the chordae tendinae, are located on the

ventricular surfaces of these cusps. These cords connect the
cusps of the valve with the papillary muscles of the
ventricular walls.
ANATOMY OF HEART
As pressure builds in the ventricular chambers,
contraction of these muscles prevents the cusps from
being forced up into the atria.

Dysfunction or rupture of the chordae tendinae,

producing regurgitation from the ventricles to the atria.
ANATOMY OF HEART
 The ARTERIAL SUPPLY of the heart muscle is derived
from the right and left coronary arteries, which arise from
the aortic sinuses .

 The left coronary artery (LCA) divides into the anterior

descending artery and the left circumflex artery.

 These arteries supply most of the left ventricle, the left

atrium, most of the ventricular septum and, in 45% of
people, the sinoatrial (SA) node.
ANATOMY OF HEART
The right coronary artery (RCA) supplies most of
the right ventricle, the atrioventricular (A V) node and,
in 55% of people, the SA node.
Innervation
 The ANS extends its influence via the vagus nerve (parasympathetic)
and upper thoracic nerves (sympathetic). These nerves mingle together
around the root and arch of the aorta near the tracheal bifurcation,
forming the cardiac plexus. Extensions from the cardiac plexus richly
supply the SA and A V nodes. They are so well-mingled that scientists
are unable to determine which nerves supply which parts of the heart.
Stimulation of the sympathetic nervous system causes acceleration of
the discharge rate in the SA node, increase in A V nodal conduction,
and increase in the contractile force of both atrial and ventricular
muscles. Stimulation of the vagus nerve causes cardiac slowing and
decreased A V nodal conduction. Thus the parasympathetic system
decelerates heart rate and the sympathetic system accelerates heart rate.
Normal impulse formation may be interrupted by vascular lesions
(occlusion of the coronary arteries) or by cardiac disease (pericarditis).
The surface markings of the heart
 The surface markings of the heart can be traced by joining
four points over the anterior chest wall. On the right, the
heart extends from the third to the sixth costal caltilages at a
distance of about to to 15 mm from the sternum. On the left,
the heart extends from the second costal cartilage to the fifth
intercostal space 12 to 15 mm, and 9 cm from the left sternal
border, respectively. Joining the two points on the left side
outlines the left atrium and ventricle. The heart is rotated to
the left in the chest, resulting in the right side of the heart
being foremost. Thus joining the two uppermost points
outlines the level of the atria and joining the two lower
points represents the margin of the right ventricle. The heart
as a whole is freely movable
CARDIAC PHYSIOLOGY
Three primary reflexes enable the heart to increase stroke
volume and cardiac output with moment-to-moment
changes in myocardial demand (French and Ct'iley, 1983).

The first reflex is the Starling Effect which refers to the

increased force of contraction that occurs with increased
venous return (preload).

The second reflex, the Anrep Effect, refers to the increase

in ventricular contractile force as a result of an increase in
atrial pressure (afterload).
CARDIAC PHYSIOLOGY
 The third, the Bowdich Effect refers to the corresponding
increase in heart rate when myocardial contractile force
increases.

 The integrated function of these three reflexes ensures that

cardiac output adjusts as demands on the heart change, that
is in health, primarily in response to exercise, body position
and emotional stress.
 CARDIAC PHYSIOLOGY
The cardiac cycle takes 0.8 second in a heart beating at 60-100
beats/min.

Ventricular systole or ejection takes about one-third of this time.

Its onset and termination are marked respectively by closure and

opening of the atrioventricular valves (mitral and tricuspid).

Diastole, or the period between successive ventricular systoles in

which the ventricles fill with blood, takes two thirds of the 0.8
second of each cardiac cycle.
CARDIAC PHYSIOLOGY
Phases of Systole and Diastole

Ventricular systole normally has three phases:

 Isovolumctric contraction period
 Rapid ejection period
 A slower ejection period.

Ventricular diastole also has three phases:

 Iso volumetric Relaxation Period
 Passive rapid filling phase
 Diastasis (a lower filling phase)
CARDIAC PHYSIOLOGY
The heart sounds are described as a low-pitched long
duration sound (SI) followed by a higher pitched
shorter duration sound that resembles the phonic
sounds of LUB-dub.

S1 is associated with closure of the atrioventricular

valves.

S2 is associated with closure of the semilunar valves.

CARDIAC PHYSIOLOGY
In inspiration, the aortic valve closes several
milliseconds before the pulmonic valve, resulting in a
splitting of the second heart sound S2.

During inspiration, intrathoracic pressure becomes

negative, more venous return and heart volume
increase, hence pulmonary ejection is prolonged in
this.
CARDIAC PHYSIOLOGY
S3 is usually associated with passive rapid filling
phase.
Abnormal in adults.
Caused by ventricular dilatation

S4 is associated with the active rapid-filling phase.

CARDIAC PHYSIOLOGY
The transport of CO2 has an important role in the acid-
base status of the blood and maintenance of normal
homeostasis (Comroe, Forster, Dubois, Briscoe, and
Carlsen, 1986).

The lung excretes 10,000 mEq of carbonic acid per

day. (Carbonic acid is broken down into water and
CO2. The CO2 is buffered and eliminated through the
lungs.)
CARDIAC PHYSIOLOGY
The kidney can excrete only 100 mEq per day of acids.
Therefore alterations in ventilation can have profound
effects on the body's acid-base status.

A decrease in the lung's ability to ventilate causes a

sharp rise in PCO2 and a drop in pH. This causes an
acute respiratory acidosis.
CARDIAC PHYSIOLOGY
If this change occurs gradually, the pH will remain within
normal limits while the PCO2 is elevated. This is known
as a compensated respiratory acidosis.

Hyperventilation causes rapid elimination of CO2 from the

blood. This results in a decreased PCO2 and an increased
pH and is known as an acute respiratory alkalosis.

Again, if the change occurs gradually, the pH remains

within normal limits even though the PCO2 is decreased.
This is a compensated respiratory alkalosis.
 Summary
Heart and diaphragm
Pericardium and its division
Layers of heart
Arterial & nerve supply of heart
Surface marking of Heart
Cardiac physiology :Starling , Anrep and Bowdich
effects
Heart sounds
Respiratory acidosis and alkalosis